Since the original observations that catecholamines are localized within neurons of the central nervous system, there has been considerable effort to associate certain behavioral functions with specific catecholamine neurons. An important rationale of these studies has been to use drugs such as amphetamine to modify both the function of catecholamine containing neurons as well as behavior and to make correlations between the effects. The mechanism of action of amphetamine is not fully understood but the net result of its action is the release of catecholamines from presynaptic sites. The release of norepinephrine, dopamine and 5-hydroxytryptamine from various regions of isolated rat brain has been characterized. Studies with norepinephrine indicate that low concentrations of amphetamine enter the neuron by the neuronal uptake process and displace norepinephrine from intraneuronal binding sites. Upon release, catecholamines interact with postsynaptic receptors to produce specific responses. It is known that the enzyme adenyl cyclase is present in brain and this enzyme has been suggested as a model for the postsynaptic catecholamine receptor. Studies in which the presynaptic nerve endings are destroyed with 6-hydroxydopamine suggest that the presynaptic nerve ending not only regulates the amount of catecholamine available to stimulate the postsynaptic enzyme but can also regulate the maximal responsiveness of the enzyme to stimulation by catecholamines.